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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 61 (1983), S. 133-138 
    ISSN: 1432-1440
    Keywords: HDL-cholesterol ; Cholestadiene ; Normal values for HDL-cholesterol ; Precipitation techniques for separation of lipoproteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The widespread use of different methods for the determination of HDL-cholesterol (in Europe: sodium phosphotungstic acid/MgCl2) in connection with enzymatic procedures (in the USA: heparin/MnCl2 followed by the Liebermann-Burchard method) but common reference values makes it necessary to evaluate not only accuracy, specificity, and precision of the precipitation step but also of the subsequent cholesterol determination. A high ratio of serum vs. concentrated precipitation reagent (10:1 V/V) leads to the formation of variable amounts of Δ-3.5-cholestadiene. This substance is not recognized by cholesterol oxidase but leads to an 1.6 times overestimation by the Liebermann-Burchard method. Therefore, errors in HDL-cholesterol determination should be considered and differences up to 30% may occur between HDL-cholesterol values determined by the different techniques (heparin/MnCl2 — Liebermann-Burchard and NaPW/MgCl2-CHOD-PAP).
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 187 (1987), S. 359-367 
    ISSN: 1433-8580
    Keywords: Nifedipine ; Atherosclerosis ; Regression ; Hypercholesterolemia ; Rabbits ; Aortic cholesterol ; Platelet half-life time
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Nifedipine has been implicated as an inhibitor of dietary induced atherosclerosis in rabbits. This study was designed to examine the effect of nifedipine on the regression of atherosclerotic lesions in this animal model. NZ-rabbits were fed a cholesterol-enriched diet (1.5%) for 4.8 months. A control group A was killed and the aorta removed for planimetry of the vessel wall lesions. The remaining animals were divided into two groups, group P receiving a placebo solution and group N a nifedipine solution (2 × 20 mg/day). They were maintained on a standard chow for a further 4.5 months. In the nifedipine-treated group N, sudanophilia of the aorta was reduced by more than 20% as compared to the cholesterol-fed control group A and was 50% lower than in the placebo-treated group. Total cholesterol of the aortic tissue was lowest in group N. No significant differences in plasma cholesterol, triglycerides or the platelet half-life time were observed between the placebo- and the nifedipine-treated group. These data indicate that nifedipine can stimulate regression of pre-existing atherosclerotic lesions in rabbits.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 172 (1978), S. 211-221 
    ISSN: 1433-8580
    Keywords: Physicochemical properties of LP-X ; Effects of bile salts ; Free fatty acids and postheparin lipolytic activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In this study it is demonstrated, that incubation of both, bile acids and free fatty acids with LP-X, the abnormal plasmalipoprotein found in patients suffering from cholestasis or LCAT-deficiency, results in striking alterations of the physico-chemical and immunological properties of LP-X: 1. The cathodic mobility in agar is changed into an anodic migration of the material. 2. The unique appearance of LP-X on electronmicrographs is altered by the incubation revealing fingerprint like structures. 3. The albumin portion of LP-X becomes immunologically detectable. 4. Bile salts cause marked changes in the hydrated density of the material as determined by zonal ultracentrifugation. 5. In vitro incubation of LP-X with postheparin plasma causes a complete disappearance of LP-X as judged by its typical migration on agar electrophoresis. All these alterations can be prevented or reversed by the addition of albumin in appropriate concentrations. These findings are important in the light of studies designed to investigate the catabolic action of plasma lipolytic enzymes on LP-X, as well as for follow up studies of LP-X concentrations during the course of disease.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1435-1803
    Keywords: ischemia ; reperfusion ; vitamin E ; infarct size ; regionalsystolic shortening
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Thirty pigs were randomly assigned to a blind treatment with vitamin E or placebo. Ten animals each received 0.5g d-alpha tocopherol intravenously before ischemia (group 1) or before reperfusion (group 2). Ten control pigs were treated with a lipid emulsion as placebo. The left anterior descending coronary artery was distally ligated for 45 min followed by 3 days of reperfusion. Infarct size was determined as ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). Regional systolic shortening was assessed by sonomicrometry. Myocardial and plasma concentrations of vitamin E were determined by high-performance liquid chromatography. Global hemodynamic parameters and estimated left ventricular oxygen consumption did not differ among the three groups. Intravenous treatment with vitamin E raised the plasma levels of this vitamin from 1 ± 0.3 mg/l (control group) to 21 ± 6 mg/l before ischemia, to 4 ± 2 mg/l before reperfusion and to 2 ± 0.6 mg/l at the end of the experiments in group 1. In group 2, vitamin E plasma levels increased from 1 ± 0.3 mg/l to 24 ± 13 mg/l before reperfusion and to 2 ± 0.6 mg/l after 3 days of reperfusion. At the end of the experiments, myocardial vitamin E concentrations amounted to 4.2 ± 0.7 ng/mg fresh weight (control group), 9.7 ± 2.1 ng/mg (group 1), and to 8.7 ± 1.4 ng/mg (group 2). The increase in vitamin E plasma concentration was not associated with a cardioprotective effect. Infarct sizes of the three groups (group 1: 68 ± 12%, group 2: 66 ± 15%, control group: 69 ± 8%) were almost identical. Furthermore, recovery of systolic shortening was not improved by the acute vitamin E treatment. Mean systolic shortening of the reperfused segment amounted to 4% in the two treatment groups and 3% in the control group after 3 days of reperfusion. These results suggest that an acute increase in vitamin E plasma concentration before ischemia or during the early phase of reperfusion does not protect the ischemic, reperfused porcine heart.
    Type of Medium: Electronic Resource
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